CAJ | 학술논문

目的探讨不同药理机制的抗抑郁对抑郁症患者电刺激痛觉诱发电位P250的影响.方法将60例不伴疼痛的抑郁症患者采用随机数字表法随机分为度洛西汀组(30例,口服度洛西汀60 mg/d)和西酞普兰组(30例,口服西酞普兰20～40 mg/d)治疗,并于治疗前、治疗第2周末测定电刺激痛觉诱发电位P250,与对照组(30名,正常健康人)进行比较;对度洛西汀组和西酞普兰组P250下降率与17项汉密尔顿抑郁量表(HAMD17)评分的相关性进行分析.结果 (1)度洛西汀组和西酞普兰组治疗前P250波幅分别为(36.4±6.8)、(35.2±6.5)μV,均高于对照组[(28.0±5.5)μV],差异有统计学意义(P均=0.000);3组P250潜伏期的差异无统计学意义(P=0.732).(2)度洛西汀组和西酞普兰组治疗第2周末P250波幅分别下降为(31.4±5.7)、(34.0±5.9)μV,均高于对照组,差异有统计学意义(P=0.020,P=0.000);2组治疗前后P250波幅的差异均有统计学意义(P=0.000,P=0.022),P250潜伏期的差异均无统计学意义(P=0.667,P=0.408).(3)度洛西汀组治疗第2周末P250波幅的下降值为(5.0±3.4)μV,下降率为(13±10)%,均高于西酞普兰组[(1.2±2.8)μV,(3±8)%],差异有统计学意义(P=0.000,P=0.000).(4)度洛西汀组和西酞普兰组治疗第2周末P250波幅下降率与HAMD17总分减分率无显著相关性(P=0.318,P=0.287),与焦虑/躯体化因子减分率呈正相关(分别r=0.370、P=0.034,r=0.417、P=0.009).结论抗抑郁药对P250波幅有下调作用,并可独立于抗抑郁效应;度洛西汀的作用强于西酞普兰.
목적 탐토불동약리궤제적항억욱대억욱증환자전자격통각유발전위P250적영향.방법 장60례불반동통적억욱증환자채용수궤수자표법수궤분위도락서정조(30례,구복도락서정60 mg/d)화서태보란조(30례,구복서태보란20～40 mg/d)치료,병우치료전、치료제2주말측정전자격통각유발전위P250,여대조조(30명,정상건강인)진행비교;대도락서정조화서태보란조P250하강솔여17항한밀이돈억욱량표(HAMD17)평분적상관성진행분석.결과 (1)도락서정조화서태보란조치료전P250파폭분별위(36.4±6.8)、(35.2±6.5)μV,균고우대조조[(28.0±5.5)μV],차이유통계학의의(P균=0.000);3조P250잠복기적차이무통계학의의(P=0.732).(2)도락서정조화서태보란조치료제2주말P250파폭분별하강위(31.4±5.7)、(34.0±5.9)μV,균고우대조조,차이유통계학의의(P=0.020,P=0.000);2조치료전후P250파폭적차이균유통계학의의(P=0.000,P=0.022),P250잠복기적차이균무통계학의의(P=0.667,P=0.408).(3)도락서정조치료제2주말P250파폭적하강치위(5.0±3.4)μV,하강솔위(13±10)%,균고우서태보란조[(1.2±2.8)μV,(3±8)%],차이유통계학의의(P=0.000,P=0.000).(4)도락서정조화서태보란조치료제2주말P250파폭하강솔여HAMD17총분감분솔무현저상관성(P=0.318,P=0.287),여초필/구체화인자감분솔정정상관(분별r=0.370、P=0.034,r=0.417、P=0.009).결론 항억욱약대P250파폭유하조작용,병가독립우항억욱효응;도락서정적작용강우서태보란.
Objective To explore effects of antidepressants with distinct pharmacological property on electrical pain-related evoked potentials P250 in depression. Methods Sixty cases pain-free depressive inpatients were randomly divided into two groups, treated with duloxetine (60 mg/d, n = 30) or citalopram (20-40 mg/d, n = 30) respectively for 2 weeks. Pain-related evoked potentials P250 was measured before and after treatment, which was contrasted with healthy controls (n=30). Results The amplitudes of P250 were significandy higher in either duloxetine or citalopram group at baseline compared with controls [(36. 4 ±6.8), (35.2±6.5)μV vs. (28.0±5.5) μV , P = 0.000, P=0.000], and decreased significantly at the end of study [(31. 4 ± 5. 7) , (34. 0 ± 5. 9) μV, P =0. 000, P =0. 022 respectively]. Either the absolutely decreased value [(5.0 ±3. 4) μV vs. (1. 2 ±2. 8) μV, P =0.000] or the decreased ratio [(13±10)% vs.(3±8)%,P = 0. 000] of P250 amplitudes were significant higher in duloxetine group than citalopram group.The reduction of P250 amplitudes was not significantly related with the change of HAMD17 total score (P = 0. 318, P = 0. 287) , which was statistically positively correlate with the reduction rate of anxiety/somatization factor in either duloxetine group or citalopram group (r = 0. 370, P = 0. 034; r = 0. 417 , P =0. 009 respectively). Conclusion Duloxetine and citalopram possibly have down-regulating effects on P250 amplitude independent of antidepressant effects, with duloxetine being more effective than citalopram.